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肌源性干細胞被稱為是衛星細胞，骨骼肌受損后能夠激活該細胞，起始增殖及分化再生出新的肌纖維。 研究發現，肌肉受損后，骨骼肌特異性microRNA miR-206在衛星細胞中明顯上調，但是它在肌肉再生中的功能還不明確。 近日，美國德克薩斯大學西南醫學中心的研究人員發現，在應答于肌肉損傷時，miR-206能夠促進骨骼肌再生。相關論文發表在5月1日的The Journal of Clinical Investigation。 他們發現，在毒素損傷的老鼠模型，miR-206的敲除會延遲再生。此外，在杜興氏肌肉營養不良的老鼠模型，miR-206的失去會加速并加重營養不良的表型。 而且，miR-206通過抑制一系列肌細胞生成的負調控因子，促進衛星細胞分化，并融合為肌肉纖維。 該研究表明，在骨骼肌再生時，miR-206對衛星細胞的分化具有決定性作用，而且miR-206能夠延遲杜興氏肌營養不良的進程，這對相關藥物開發及疾病研究提供了新的思路。（生物谷Deepblue編譯） microRNA-206 promotes skeletal muscle regeneration and delays progression of Duchenne muscular dystrophy in mice Ning Liu, Andrew H. Williams, Johanna M. Maxeiner, Svetlana Bezprozvannaya, John M. Shelton, James A. Richardson, Rhonda. Skeletal muscle injury activates adult myogenic stem cells, known as satellite cells, to initiate proliferation and differentiation to regenerate new muscle fibers.The skeletal muscle–specific microRNA miR-206 is upregulated in satellite cells following muscle injury, but its role in muscle regeneration has not been defined.Here, we show that miR-206 promotes skeletal muscle regeneration in response to injury. Genetic deletion of miR-206 in mice substantially delayed regeneration induced by cardiotoxin injury.Furthermore, loss of miR-206 accelerated and exacerbated the dystrophic phenotype in a mouse model of Duchenne muscular dystrophy.We found that miR-206 acts to promote satellite cell differentiation and fusion into muscle fibers through suppressing a collection of negative regulators of myogenesis. Our findings reveal an essential role for miR-206 in satellite cell differentiation during skeletal muscle regeneration and indicate that miR-206 slows progression of Duchenne muscular dystroph. |
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